From 1958 through 1992 a total of 3603 patients underwent surgery for esophageal squamous cell carcinoma in our department. Among these patients 3099 resections were performed, for an overall resectability of 86.0%. Of the resections, 2341 (75.5%) were classified as curative and 758 (24.5%) palliative. The overall morbidity and 30-day mortality rates were 23.4% and 3.8%, respectively. For resected cases the mortality was 4.0%. The more than 5-year follow-up rate of patients with resection was 97%. The actual 5-, 10-, and 15-year survival rates were 30.4%, 23.6%, and 17.9%, respectively. Recurrence or metastasis remained the cause of death in 60.9% and 25.5% of patients who lived longer than 5 years and 15 years, respectively, after operation. The TNM staging, lymph node metastasis, extra-esophageal invasion, tumor differentiation, tumor length, and category of operation were major determinants influencing long-term prognosis. The left thoracotomy approach was used exclusively in 2613 cases (84.3% of all resected cases) in which intrathoracic resections and anastomoses were performed. The stomach was used as a substitute for the esophagus in 98.8% of the resected cases compared with 1.2% colon transplants. The former procedure was far safer than the latter. Above-average results presented in this paper support the surgical policy we have pursued thus far: to resect the primary tumor by partial or subtotal esophagectomy and to remove all lymph nodes wherever they were found in all patients with disease earlier than stage III. Early detection and early treatment no doubt are the only ways to materially improve the long-term surgical results.

Allergic rhinitis (AR) is the most common cause of inflammation of the nasal mucosa. It is also the most common form of non-infectious rhinitis associated with an immunoglobulin E (IgE)-mediated immune response against allergens. Previous studies have indicated that interleukin-1β (IL-1β) has a pathological role in the development of allergic asthma. The present study was designed to assess whether IL-1β participates in the pathogenesis of AR. A total of 45 patients with AR were enrolled in the present study and were identified to have increased IL-1β expression expressed by peripheral blood mononuclear cells (PBMCs), and the mitochondrial reactive oxygen species (ROS) and NLRP3 are required for IL-1β synthesis in monocytes/macrophages and PBMCs from patients with AR. The levels of IL-1β and interleukin-17 (IL-17) were increased in patients with AR and were positively correlated with each other. The results of the present study suggested that patients with AR have raised mitochondrial ROS levels, which may upregulate the expression of IL-1β, affecting IL-17-production and serving a role in the pathogenesis of AR.

Background Although the clinical efficacy and safety of repetitive transcranial magnetic stimulation (rTMS) in the treatment of chronic tinnitus have been frequently examined, the results remain contradictory. Therefore, we performed a systematic review and meta-analysed clinical trials examining the effects of rTMS to evaluate its clinical efficacy and safety. Methods Studies of rTMS for chronic tinnitus were retrieved from PubMed, Embase, and Cochrane Library through April 2020. Review Manager 5.3 software was employed for data synthesis, and Stata 13.0 software was used for analyses of publication bias and sensitivity. Results Twenty-nine randomized studies involving 1228 chronic tinnitus patients were included. Compared with sham-rTMS, rTMS exhibited significant improvements in the tinnitus handicap inventory (THI) scores at 1 week (mean difference [MD]: − 7.92, 95% confidence interval [CI]: − 14.18, − 1.66), 1 month (MD: -8.52, 95% CI: − 12.49, − 4.55), and 6 months (MD: -6.53, 95% CI: − 11.406, − 1.66) post intervention; there were significant mean changes in THI scores at 1 month (MD: -14.86, 95% CI: − 21.42, − 8.29) and 6 months (MD: -16.37, 95% CI: − 20.64, − 12.11) post intervention, and the tinnitus questionnaire (TQ) score at 1 week post intervention (MD: -8.54, 95% CI: − 15.56, − 1.52). Nonsignificant efficacy of rTMS was found regarding the THI score 2 weeks post intervention (MD: -1.51, 95% CI: − 13.42, − 10.40); the mean change in TQ scores 1 month post intervention (MD: -3.67, 95% CI: − 8.56, 1.22); TQ scores 1 (MD: -8.97, 95% CI: − 20.41, 2.48) and 6 months (MD: -7.02, 95% CI: − 18.18, 4.13) post intervention; and adverse events (odds ratios [OR]: 1.11, 95% CI: 0.51, 2.42). Egger’s and Begg’s tests indicated no publication bias (P = 0.925). Conclusion This meta-analysis demonstrated that rTMS is effective for chronic tinnitus; however, its safety needs more validation. Restrained by the insufficient number of included studies and the small sample size, more large randomized double-blind multi-centre trials are needed for further verification.

Cisplatin-induced ototoxicity is one of the major adverse effects in cisplatin chemotherapy, and hearing protective approaches are unavailable in clinical practice. Recent work unveiled a critical role of autophagy in cell survival in various types of hearing loss. Since the excessive activation of autophagy can contribute to apoptotic cell death, whether the activation of autophagy increases or decreases the rate of cell death in CDDP ototoxicity is still being debated. In this study, we showed that CDDP induced activation of autophagy in the auditory cell HEI-OC1 at the early stage. We then used rapamycin, an autophagy activator, to increase the autophagy activity, and found that the cell death significantly decreased after CDDP injury. In contrast, treatment with the autophagy inhibitor 3-methyladenine (3-MA) significantly increased cell death. In accordance with in vitro results, rapamycin alleviated CDDP-induced death of hair cells in zebrafish lateral line and cochlear hair cells in mice. Notably, we found that CDDP-induced increase of Sirtuin 1 (SIRT1) in the HEI-OC1 cells modulated the autophagy function. The specific SIRT1 activator SRT1720 could successfully protect against CDDP-induced cell loss in HEI-OC1 cells, zebrafish lateral line, and mice cochlea. These findings suggest that SIRT1 and autophagy activation can be suggested as potential therapeutic strategies for the treatment of CDDP-induced ototoxicity.